الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Inflammatory bowel disease comprises primarily two major subphenotypes, Crohn’s disease (CD) and ulcerative colitis (UC). CD is an idiopathic, relapsing chronic inflammatory disease of the gastrointestinal tract. CD affects the entire GIT from mouth to anus in a discontinuous and transmural way. Unlike CD, UC is confined to the mucosa and restricted to the large bowel. The etiology of IBD is multifactorial including genetic susceptibility, host immunity and environmental factors.
The diagnosis of inflammatory bowel disease (IBD) and the differentiation between ulcerative colitis and Crohn’s disease is currently based on the combination of clinical, laboratory, radiological, endoscopic and histopathologic criteria.
In the normal intestine the immunologic tone is one of tolerance or suppression of immune responses against non-pathogens in the gut lumen. These non-pathogens include both commensal flora and dietary antigens. In IBD there is growing evidence that this tolerant state, at least to specific components of the flora, is lost (the presence of ANCA and ASCA serum antibodies is evidence for loss of tolerance). ASCA is part of the family of anti-glycan (carbohydrate) antibodies, of value in differentiating between UC and CD. There is a pressing need to develop new seromarkers that will serve as diagnostics and prognostic tools.
Glycans are sugars associated with proteins, abundant on many living cells (micro-organisms, immune cells, erythrocytes, and tissue matrices). The anti-glycan antibodies are directed against laminaribioside, chitobioside and mannobioside residues and are designated anti- laminaribioside carbohydrate antibodies (ALCA), anti-chitobioside carbohydrate antibodies (ACCA), anti-mannobioside carbohydrate antibodies (AMCA) and gASCA, respectively. Anti-laminarin IgA (Anti-L), and anti-chitin IgA (Anti-C) are new members of this family.
The present study included 100 patients : 80 IBD patients (50 CD and 30 UC) and 20 patients with gastrointestinal symptoms, proved not to be IBD. We evaluated inflammatory markers (ESR, CRP), complete blood count, seromarkers ( ASCA, P-ANCA, ALCA, ACCA and AMCA), radiologic examination in all groups. Endoscopic and histopathologic examinations were done in IBD patients.
The aim of the work is to assess the prevalence of the new serological markers (antiglycan antibodies) in IBD patients, and to study their role in the diagnosis and differential diagnosis of IBD, as well as the possible interaction with the clinical presentation.
The present study showed, the tested markers were highly specific for CD (95%-100%) but have low sensitivities. However, the combined use of the markers increases sensitivities.
We found that 37.5% of ASCA negative patients were positive to at least one of the new serological markers; these results suggest that ASCA negative patients represent a distinct immunological phenotypic group. We confirmed the additional value of ALCA, ACCA and AMCA in the diagnosis of CD.
Using Roc analysis, ASCA IgG, ALCA and AMCA were able to differentiate between CD and controls (AUC=0.684, 0.736 and 0.697 respectively). ALCA and ACCA were able to differentiate between CD and UC (AUC=0.728 and 0.703 respectively).
We studied the markers both quantitatively and qualitatively. There was a significant association between ASCA IgG, ALCA and AMCA positivity and upper GI involvement in CD patients (p= 0.037, 0.0015 and 0.006 respectively) there was a significant association between ALCA and AMCA positivity and complicated disease behavior (p=0.001 and 0.035 respectively) also between ALCA positivity and perianal disease (p=0.040) and between both ASCA IgG and IgA positivity and need for surgery.